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Coronin 1B regulates the TNFa-induced apoptosis of HUVECs by mediating the interaction between ...
  • Date2021-02-23 16:46
  • Update2021-02-23 16:46
  • CountersignatureDivision of Research Planning
  • Tel043-719-8033

Biochemical and Biophysical Research Communications, 2020.526, 999-1004, DOI: https://doi.org/10.1016/j.bbrc.2020.03.096


Coronin 1B regulates the TNFa-induced apoptosis of HUVECs by mediating the interaction between TRADD and FADD mediating the interaction between TRADD and FADD

Geun-Young Kim, Hyun-Joung Lim; Won-Ho Kim; Hyun-Young Park


Abstract

    Coronin 1B is an actin-binding protein that plays important roles in actin-dependent cellular processes. We previously reported that coronin 1B is involved in vascular endothelial cell growth factoreinduced migration of human umbilical vein endothelial cells (HUVECs). However, the role of coronin 1B in tumor necrosis factor alpha (TNFa)-induced endothelial cell apoptosis remained unknown. In this study, we investigated whether coronin 1B affects TNFa-induced HUVEC apoptosis and sought to elucidate the mechanism by which coronin 1B regulates this cellular process. Depletion of coronin 1B by siRNA transfection decreased TNFa-induced apoptosis of HUVECs, as determined by MTT, terminal deoxynucleotidyl transferase dUTP nick end labeling and caspase-3 activity assays. Coronin 1B depletion also decreased caspase-8 cleavage via a JNK-independent pathway. Coronin 1B interacted with Fas-associated death domain protein (FADD) in both a plasmid overexpression system in HEK293T cells and at the endogenous protein level in TNFa-stimulated HUVECs. Immunoprecipitation and in situ proximity ligation assays showed that coronin 1B depletion diminished the interaction between TNFa-induced TNF receptor-1-associated death domain protein (TRADD) and FADD, suggesting that coronin 1B is required for the TNFa-induced TRADD and FADD interaction and subsequent caspase-8/caspase-3 cascade activation, ultimately leading to apoptosis.



  • 본 연구는 질병관리본부 연구개발과제연구비를 지원받아 수행되었습니다.
  • This research was supported by a fund by Research of Korea Centers for Disease Control and Prevention.


This public work may be used under the terms of the public interest source This public work may be used under the terms of the public interest source
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